Anti-C5/C5a Antibody Picoband®

C5a is a protein fragment released from complement component C5. This gene is mapped to 9q33.2. The protein encoded by this gene is the fifth component of complement, which plays an important role in inflammatory and cell killing processes. This protein is comprised of alpha and beta polypeptide chains that are linked by a disulfide bridge. An activation peptide, C5a, which is an anaphylatoxin that possesses potent spasmogenic and chemotactic activity, is derived from the alpha polypeptide via cleavage with a convertase. The C5b macromolecular cleavage product can form a complex with the C6 complement component, and this complex is the basis for formation of the membrane attack complex, which includes additional complement components. Mutations in this gene cause complement component 5 deficiency, a disease where patients show a propensity for severe recurrent infections. Defects in this gene have also been linked to susceptibility to liver fibrosis and to rheumatoid arthritis.

Cancer, Cell Biology, Cell Cycle, Cell Cycle Inhibitors, Cell Division, Cytokinesis, DNA/RNA, DNA Damage & Repair, DNA Damage Response, Epigenetics and Nuclear Signaling, MAPK Pathway, p53 Pathway, Protein Phosphorylation, Ser/Thr Kinases, Signal Transduction

Derived from proteolytic degradation of complement C5, C5 anaphylatoxin is a mediator of local inflammatory process. Binding to the receptor C5AR1 induces a variety of responses including intracellular calcium release, contraction of smooth muscle, increased vascular permeability, and histamine release from mast cells and basophilic leukocytes. C5a is also a potent chemokine which stimulates the locomotion of polymorphonuclear leukocytes and s their migration toward sites of inflammation. .

1. Delgado-Cervino, E., Fontan, G., Lopez-Trascara, M. C5 complement deficiency in a Spanish family: molecular characterization of the double mutation responsible for the defect. Molec. Immun. 42: 105-111, 2005. 2. Pfarr, N., Prawitt, D., Kirschfink, M., Schroff, C., Knuf, M., Habermehl, P., Mannhardt, W., Zepp, F., Fairbrother, W. G., Loos, M., Burge, C. B., Pohlenz, J. Linking C5 deficiency to an exonic splicer enhancer mutation. J. Immun. 174: 4172-4177, 2005. Note: Erratum: J. Immun. 182: 5152 only, 2009.

Store at -20°C for one year from date of receipt. After reconstitution, at 4°C for one month. It can also be aliquotted and stored frozen at -20°C for six months. Avoid repeated freeze-thaw cycles.